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能够介导寄生虫特异性迟发型超敏反应的L3T4 + T细胞在实验性恰加斯病的病理过程中起作用。

L3T4+ T cells able to mediate parasite-specific delayed-type hypersensitivity play a role in the pathology of experimental Chagas' disease.

作者信息

Hontebeyrie-Joskowicz M, Said G, Milon G, Marchal G, Eisen H

出版信息

Eur J Immunol. 1987 Jul;17(7):1027-33. doi: 10.1002/eji.1830170720.

DOI:10.1002/eji.1830170720
PMID:2440690
Abstract

During the chronic phase of infection with the parasite Trypanosoma cruzi, mice develop inflammatory lesions in the heart and skeletal muscles, as well as in peripheral nerves and the liver. We demonstrated the presence, in the blood of chronically infected mice, of L3T4+ T cells able to transfer a specific T. cruzi delayed-type hypersensitivity (DTH) reaction. Transfer of the chronic inflammatory lesions was obtained by injecting Lyt-2+-depleted lymphocytes from either lymph node or blood of infected mice. T cell lines were established from the chronically infected mice by culturing peripheral blood lymphocytes or lymph node cells with either T. cruzi extracts (TC) or mouse peripheral nerve extracts (PN). Those cell lines that presented an L3T4+ phenotype were also able to specifically transfer a local DTH reaction to naive recipients. Examination of the antigen specificities of these TDTH lines revealed three types: those that mediated a DTH reaction to TC, those that responded to both TC and PN and those that provoked a DTH response when injected with subinflammatory doses of an irrelevant antigen. Some of the lines, when injected into the sciatic nerve of naive recipients, provoked demyelination of the type observed in chronically infected animals. These results suggest that T. cruzi and the host nervous system share common epitopes that can be recognized by TDTH cells.

摘要

在感染克氏锥虫的慢性期,小鼠的心脏、骨骼肌、外周神经和肝脏会出现炎症性病变。我们证明,在慢性感染小鼠的血液中存在能够传递特定克氏锥虫迟发型超敏反应(DTH)的L3T4 + T细胞。通过注射来自感染小鼠淋巴结或血液中去除Lyt-2 +的淋巴细胞,可实现慢性炎症性病变的转移。通过用克氏锥虫提取物(TC)或小鼠外周神经提取物(PN)培养慢性感染小鼠的外周血淋巴细胞或淋巴结细胞,建立了T细胞系。那些呈现L3T4 +表型的细胞系也能够将局部DTH反应特异性地传递给未感染的受体。对这些TDTH系的抗原特异性检查揭示了三种类型:介导对TC的DTH反应的细胞系、对TC和PN均有反应的细胞系以及在注射亚炎症剂量的无关抗原时引发DTH反应的细胞系。当将其中一些细胞系注射到未感染受体的坐骨神经中时,会引发在慢性感染动物中观察到的那种脱髓鞘现象。这些结果表明,克氏锥虫和宿主神经系统共享可被TDTH细胞识别的共同表位。

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1
L3T4+ T cells able to mediate parasite-specific delayed-type hypersensitivity play a role in the pathology of experimental Chagas' disease.能够介导寄生虫特异性迟发型超敏反应的L3T4 + T细胞在实验性恰加斯病的病理过程中起作用。
Eur J Immunol. 1987 Jul;17(7):1027-33. doi: 10.1002/eji.1830170720.
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[Immune response to Trypanosoma cruzi. An approach to the pathogenesis of Chagas' disease].[对克氏锥虫的免疫反应。恰加斯病发病机制的一种研究方法]
Acta Physiol Pharmacol Latinoam. 1985;35(1):1-47.

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The SA85-1.1 protein of the Trypanosoma cruzi trans-sialidase superfamily is a dominant T-cell antigen.克氏锥虫转唾液酸酶超家族的SA85-1.1蛋白是一种主要的T细胞抗原。
Infect Immun. 2000 Jun;68(6):3574-80. doi: 10.1128/IAI.68.6.3574-3580.2000.
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Chagas' disease and the autoimmunity hypothesis.恰加斯病与自身免疫假说。
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Circulating antibodies against nicotinic acetylcholine receptors in chagasic patients.恰加斯病患者体内抗烟碱型乙酰胆碱受体的循环抗体。
Clin Exp Immunol. 1997 Nov;110(2):219-25. doi: 10.1111/j.1365-2249.1997.tb08320.x.
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Interleukin-12-mediated resistance to Trypanosoma cruzi is dependent on tumor necrosis factor alpha and gamma interferon.白细胞介素-12介导的对克氏锥虫的抗性依赖于肿瘤坏死因子α和γ干扰素。
Infect Immun. 1996 Jul;64(7):2381-6. doi: 10.1128/iai.64.7.2381-2386.1996.
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Chagas' disease is attenuated in mice lacking gamma delta T cells.在缺乏γδ T细胞的小鼠中,恰加斯病病情减轻。
Infect Immun. 1996 Jan;64(1):215-21. doi: 10.1128/iai.64.1.215-221.1996.
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Depletion of T-cell subpopulations results in exacerbation of myocarditis and parasitism in experimental Chagas' disease.T细胞亚群的耗竭会导致实验性恰加斯病中心肌炎和寄生虫感染的加重。
Infect Immun. 1994 May;62(5):1820-9. doi: 10.1128/iai.62.5.1820-1829.1994.
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Trypanosoma cruzi infection enhances polyreactive antibody response in an acute case of human Chagas' disease.克氏锥虫感染增强了人类恰加斯病急性病例中的多反应性抗体反应。
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